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61,005 resultsShowing papers similar to Multiomics RevealsNonphagocytosable MicroplasticsInduce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactionsand Barrier Dysfunction
ClearMultiomics Reveals Nonphagocytosable Microplastics Induce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactions and Barrier Dysfunction
Researchers used multi-omics analysis to understand how large microplastics that cannot be absorbed by intestinal cells still cause colon inflammation in mice. They found that long-term oral exposure to polystyrene microplastics disrupted bile acid metabolism and gut barrier function, leading to the accumulation of specific bile acids that triggered cell death in colon tissue. The study reveals a novel mechanism linking microplastic exposure to intestinal inflammation through bile acid-gut microbiota interactions.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers induced colitis in mice using dextran sodium sulfate and orally administered polystyrene micro- and nanoplastics of three sizes, then tracked biodistribution, macrophage polarization, and gut microbiome changes. In colitis conditions, microplastic uptake into systemic tissues was enhanced, macrophages shifted toward a pro-inflammatory phenotype, and gut microbial diversity decreased, suggesting that inflammatory bowel disease increases vulnerability to microplastic-driven systemic harm.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers exposed colitis mouse models to polystyrene micro- and nanoplastics to test whether MNP exposure worsens inflammatory bowel disease, finding that MNPs altered biodistribution and exacerbated inflammatory responses in animals with pre-existing gut inflammation.
Polystyrene micro- and nanoplastics aggravates colitis in a mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers found that polystyrene micro- and nanoplastics aggravated colitis symptoms in a mouse model, increasing gut permeability, inflammatory cytokine levels, and tissue damage compared to controls. The study provides mechanistic evidence linking microplastic exposure to worsening of inflammatory bowel conditions.
Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis
Researchers fed polystyrene microplastics to mice for six weeks and found that healthy mice developed changes in their colon lining, including altered mucus composition and immune cell populations. When mice with experimentally induced colitis also consumed microplastics, their intestinal inflammation was significantly more severe. The study suggests that microplastic exposure may worsen inflammatory bowel conditions.
Effects induced by polyethylene microplastics oral exposure on colon mucin release, inflammation, gut microflora composition and metabolism in mice
Researchers fed mice polyethylene microplastics for 30 days and found that even low doses reduced protective mucus in the colon, altered inflammation markers, and shifted the composition of gut bacteria. The microplastics increased the ratio of Bacteroides to Firmicutes bacteria and affected metabolic pathways in the gut microbiome. The study suggests that oral microplastic exposure may disrupt intestinal health by modifying the gut microbial community and its metabolism.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome
Mice were orally exposed to a mixed polystyrene, polyethylene, and PLGA microplastic suspension for several weeks and gut microbiome composition and metabolomics were analyzed. Mixed microplastic exposure shifted the gut microbiome toward dysbiotic profiles in both male and female mice, with accompanying metabolome changes related to lipid and amino acid metabolism.
Orally Ingested Micro- and Nano-Plastics: A Hidden Driver of Inflammatory Bowel Disease and Colorectal Cancer.
This review synthesizes evidence linking ingested micro- and nano-plastics to inflammatory bowel disease and colorectal cancer risk, proposing that microplastics act as a hidden driver of gut inflammation in vulnerable populations. The authors argue that intestinal accumulation of microplastics triggers immune and oxidative stress pathways that contribute to disease progression.
Ingestion of micro- and nanoplastic perturbs tissue homeostasis and macrophage core functions
Researchers fed mice polystyrene particles chronically and found that micro- and nanoplastics breached intestinal barriers and accumulated in multiple organs, disrupting tissue homeostasis and impairing core macrophage functions including phagocytosis and inflammatory regulation.
Polystyrene micro- and nanoplastics in a colitis mouse model – effects on biodistribution, macrophage polarization, and gut microbiome
Researchers studied the effects of polystyrene micro- and nanoplastics in a mouse model of colitis, examining biodistribution, immune cell responses, and gut microbiome changes. The study found that nanosized particles in particular showed distinct biodistribution patterns and affected macrophage polarization under inflammatory conditions, suggesting that intestinal inflammation may alter how the body handles micro- and nanoplastic particles.
Microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils
Researchers administered polystyrene microplastics orally to mice and then assessed distribution and immune cell interactions in both mice and human cells. Both 1 µm and 10 µm particles crossed the intestinal epithelium and were detected in blood and liver after 10 days, and human monocytes and neutrophils that ingested the particles underwent inflammatory cell death.
Distinctive metabolic disturbances associated with redox homeostasis, nervous and hormonal functions during gut microbial enrichment upon polystyrene microplastic exposure
Researchers tracked gut microbial enrichment, virome shifts, and metabolomic changes in organisms exposed to polystyrene microplastics, finding Eubacteriales-dominated dysbiosis accompanied by colitis. Microplastic exposure activated polyamine synthesis pathways, altered serotonin and thyroxine metabolism, and increased cholesterol-derived hormone synthesis, revealing complex hormonal and neurochemical disruption.
UnravelingPersistent Health Impacts in Mice FollowingCessation of Microplastic Exposure: Insights beyond the Surface
Mice were fed polystyrene microplastics (40-100 µm) at environmentally relevant or 10x doses for 21 weeks, then monitored for four weeks after exposure ceased. Despite stopping exposure, lipid metabolism disruption and gut microbiota dysbiosis persisted at high doses, indicating that microplastic-induced health impacts may not fully reverse after cessation.
Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks
Researchers found that two weeks of oral polystyrene microplastic exposure in ICR mice induced an inflammatory response specifically in the mid colon, suggesting microplastics may contribute to colonic inflammation.
Microplastic consumption induces inflammatory signatures in the colon and prolongs a viral arthritis
Mice that consumed low doses of polystyrene microplastics showed signs of colon inflammation and experienced prolonged viral arthritis symptoms. The results suggest that microplastic ingestion may worsen inflammatory conditions, though more research is needed to confirm human relevance.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota
Rats exposed to polystyrene microplastics for 90 days developed significant colon inflammation, including damaged gut lining, increased inflammatory markers, and disrupted gut bacteria. The study identified a specific inflammatory pathway (TLR4/NF-kB/COX-2) through which microplastics trigger intestinal inflammation, providing important clues about how plastic particles in food and water could contribute to gut diseases in humans.
Effects of partial reduction of polystyrene micro-nanoplastics on the immunity, gut microbiota and metabolome of mice
This mouse study examined whether partial gut degradation of polystyrene micro- and nanoplastics affects immune markers, gut microbiota, and metabolome, finding that nanoplastic exposure produced distinct immune and microbial changes compared to microplastic exposure. Notably, different exposure doses shifted the key bacterial species stabilizing gut microbial networks.
Polystyrene microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils
Researchers orally administered 1 μm and 10 μm polystyrene particles to mice for 10 days and found that both sizes crossed the intestinal epithelium and were detected in blood and liver; when phagocytosed by human monocytes and neutrophils, the particles triggered complement-dependent inflammatory cell death.
Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway
Mice that swallowed polystyrene microplastics for 28 days developed oxidative stress and inflammation in their colons, leading to a weakened intestinal barrier with reduced protective mucus and loosened cell connections. The largest microplastics (5 micrometers) caused the most severe gut damage through a specific inflammatory pathway (NF-kB/NLRP3/MLCK), and antioxidant treatment was able to partially reverse the effects.
Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice
Researchers gave mice polypropylene microplastics (smaller than 10 micrometers) by mouth for 28 days and found significant damage to the colon, including inflammation, destruction of the gut barrier, and increased cell death. The smaller particles caused more severe damage than larger ones, triggering an inflammatory pathway that broke down the protective lining of the intestine. This is one of the first studies on polypropylene, the most common plastic found in human tissue, showing it can damage the gut at sizes small enough to be absorbed by the body.
Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage
In a mouse study, polystyrene nanoplastics accelerated the development of colon cancer linked to inflammatory bowel disease by disrupting fat metabolism and causing DNA damage in intestinal cells. The nanoplastics also altered gut bacteria and increased intestinal inflammation, suggesting that plastic particle exposure could worsen outcomes for people already at risk for colon cancer.
Polystyrene nanoplastics readily penetrate intestine and cause sex-specific effects mediated by bile acids and microbiome
Researchers found that approximately 60% of ingested polystyrene nanoparticles cross the intestine wall within three hours in mice, with most then captured by the liver and discharged via the biliary system. The study revealed significant sex differences, with male mice being more sensitive than females, and showed that nanoparticle exposure disrupts bile acid metabolism and increases susceptibility to colitis by altering gut bacteria.